The cry-it-out debate

Stress, cortisol, crying – what’s the big deal?

I’ve been trying for some time to formulate a coherent response to recent books which continue to say that cry-it-out is not harmful (Oster, 2019; Canapari, 2019). Even public guidelines for children’s community services have jumped on the band wagon (Asmussen and Brims, 2018). But what is the truth? How is anyone supposed to make an informed decision if they cannot interpret the research? I’m going to attempt to walk you through the current evidence-base.

The central argument is between opposing camps:

Cry it out (or variations of it) is safe, quick, and effective

Vs

Cry it out is potentially harmful and doesn’t always work

These are important questions to ask. After all, if there is a quick and effective method to help everyone get more sleep – that’s awesome. On the other hand, if it becomes apparent that there is a downside – we need to know that too.

This is a highly emotive debate, with both sides at times getting pretty hot under the collar. I totally understand this – after all, we all hate being told that we might be doing something that is not recommended. But the real issue is whether we can trust the research that we currently have.

There have been a number of studies attempting to help us figure this out. I’ll try to be brief, and objective. This is not intended to be a sanctimonious piece!

The currently available research studies

First off, we had the Hiscock study. 328 mother-baby pairs aged 8-10 months. The research was actually attempting to find out whether controlled crying (CC) was effective, and whether it reduced maternal mental health problems. Key findings included:

There was no significant difference in night waking and sleep outcome between the CC group and the control group

There was a statistically significant reduction in maternal mental health problems in the CC group (even though the sleep did not improve)

Then we had the Middlemiss study. 25 mother-baby pairs aged 4-10 months. The research was examining cortisol levels in both mothers and babies during cry-it-out (CIO). The research team sought to find out whether infants and parents stress responses would be synchronized. Cortisol samples were taken before sleep training and 20 minutes after sleep onset on the first and third day of sleep training. Key findings included:

Maternal cortisol levels decreased when babies stopped crying and went to sleep.

Shortly afterward, we had the follow up of the Hiscock study – the Price study. This study took cortisol samples of the children from the original sample when the children were 6 years old. Key findings included:

All the cortisol samples were within the normal range

Finally, we have the Gradisar study. 43 mother-baby pairs aged 6-16 months. The researchers measured cortisol before the intervention, and then 12 months afterwards. They also used the Strange Situation test (Ainsworth & Bowlby, 1991) to ascertain whether the children had a secure or insecure attachment. Key findings:

All cortisol samples were within the normal range

There was not a statistically significant difference in coding for attachment type between the CC group and controls (39% insecure in control group, and 46% insecure in CC group)

The overwhelming consensus from popular books, media, sleep research, and even our UK public health guidelines has been to suggest that these studies are evidence that CC is not harmful and should therefore be recommended as a safe, effective and quick behavioural sleep strategy to improve infant sleep.

But is it?

Firstly, it is important to note that the Hiscock study did not find that sleep training actually improved the sleep. The main conclusion of this study was that CC reduced the risk of maternal depression. Another study also found that behavioural sleep training does not work in infants (Douglas and Hill, 2013). Anecdotally, many people report that sleep training involving leaving infants to cry sometimes initially seems to reduce night waking, but then the intervention may need to be repeated – sometimes more than once.

Secondly, all of the studies have been criticized for a variety of reasons. The Price study had a large loss to follow up, was not a representative sample, and did not take a baseline cortisol sample – so we cannot compare the children’s samples against a pre-intervention sample. The Gradisar study was very small, and only had about 14 children in each of the 3 groups for comparison. In addition, they used the Strange Situation test on the children 12 months after the intervention. Some of the children would have been outside of the age range at which the test is considered valid and reliable. Finally, this study had a disproportionate number of insecurely attached children, which suggests that the sample was either self-selecting and indicated prior problems (Belanger et al, 2015), or was a non-representative sample. It is not usual to find that almost half your sample are coded as insecurely attached. The Middlemiss study has equally been critiqued by people who have said that CIO was an inappropriate intervention for the youngest babies in that particular sample, and therefore the cortisol response may have been high because they used the wrong intervention. The Middlemiss sample was also small – though in its defense, they were testing for asynchrony of maternal-infant stress response, rather than exploring CIO to assess for the impact on stress response per se.

Finally, let’s think about cortisol. The assumption made in the Price and Gradisar studies is that cortisol is a robust measure of whether the intervention studied has negatively affected the stress response. In fact, this is a really important assumption, and has a number of implications on the research interpretation. Let’s dig in to cortisol a little further…

What is the cortisol response?

Cortisol has a number of important functions. Our stress response is crucial, because it helps us react to threats. A healthy stress response with be mounted appropriately, and then fall once the threat has passed.

Cortisol is also a circadian hormone, fluctuating throughout the day, affecting our levels of concentration and alertness. It has some other functions, which are less relevant in the context of the sleep and stress debate – so I won’t bore you!

Essentially, you have a circadian linked cortisol profile, which will vary with the time of day. You also have a separate mechanism – your stress-linked cortisol response, which is not circadian linked. This makes total sense, because otherwise, if we were exposed to threat or danger at a time when our circadian cortisol level was low, we would be unable to react. That would be a serious design fault!

What about normal circadian cortisol levels?

Cortisol levels actually fluctuate quite a lot. It seems to take an infant about 4 weeks to have circadian control of cortisol, and then cortisol levels rise month on month until an infant is about 12 months (Ivars et al, 2015). Cortisol values then fall between the ages of 1-6 years (Simons et al, 2015). Cortisol values also fluctuate over the course of a day, and in response to the natural circadian rhythm. So, people with early bird chronotypes will have a differently timed circadian cortisol profile to people with night owl chronotypes (Bailey and Heitkemper, 2001). The lowest value will naturally be about 3-5 hours after sleep onset, and the highest value will be in the morning, soon after waking.

One of the important points about this is that it would be difficult to compare the children in the studies against a reference value of cortisol as cortisol values will change with age. So although they controlled for time of day, there is sparse information about whether they controlled for cortisol levels by age.

But how different is the stress response from the circadian levels of cortisol, and does it matter?

Well, this is a good question. Is the circadian cortisol value a good indicator of the stress cortisol value? The studies that have explored this have largely assumed that if a child’s cortisol sample is within normal range, that they have not got an elevated stress response. The Price study checked cortisol samples 6 years after the intervention. The Gradisar study took cortisol samples at a few intervals after the intervention, at one week, one month and three months after the sleep training or control group. However, recent research has found that there is no association between the circadian cortisol level and a stress cortisol response (Simons et al, 2017). The hugely significant aspect of this point is that in the Price and Gradisar studies, the assumption is that because the cortisol values are normal, that the child has a normal stress response. But they checked the circadian cortisol value, which is independent of the stress response.

The Gradisar study, in fairness, does acknowledge its limitations of being a small sample, and not checking a cortisol sample during an intervention. The researchers also notice the drop in circadian cortisol over time – consistent with the findings by Simons et al (2015) and Ivars et al (2015) that cortisol values change over time – reducing between the ages of 1-6 years. The point about this is that if you check a cortisol sample at baseline, and then 3 months or 6 years later, it will have decreased. This has nothing at all to do with a stress response though, and everything to do with normal circadian cortisol fluctuations. So, using this as a reassuring finding is misleading.

How is the cortisol stress response affected by early parenting?

Our cells need to be primed to respond to cortisol. One of the ways we can do this is through glucocorticoid receptors (GRs). GRs attach themselves to cortisol and this allows the activated GR complex to enter a cell and interact with it, including its’ DNA. Now, before any confusion is caused – GRs are the good guys! GRs enable us to respond efficiently to stress. The more GRs we have, the more sensitive we are to cortisol – meaning we need to release less cortisol to have an effective stress response. It also means we can recover faster from stress. All good news so far.

If we have fewer GRs, we need more cortisol to have the same effective stress response, and we also have a slower recovery from stress.

It appears that close, nurturing, responsive care in infancy is linked with an upregulation of an epigenetic process that causes more GRs to be produced. The change is stable and permanently affects our stress response (Mclaughlin et al, 2015). In fact, insecure attachment is linked with highly disorganized sleep – so anything we can do to optimize attachment is likely to have a beneficial effect (Belanger et al, 2015).

In contrast, a lack of responsive care causes the gene that is responsible for making GRs to be switched off (methylated if you want the official word!). The child will have fewer GRs, and therefore will have an elevated stress response and slower recovery from stress (Francis and Meaney, 1999).

What’s the implication?

Well, lots of research is based on children in abusive or highly toxic or stressful situations. It may not be fair to compare the outcomes of those children with those undergoing sleep training. In fact, doing this has tended to aggravate people and cause a particularly divisive argument. Some people have previously tried to dissuade others from sleep training, citing research studies on neglected children as evidence that a non-response causes attachment and neurological problems. But the counter-argument to this is that if a child lives in the context of a close, loving family, with responsive parents and is securely attached, how can you compare the two environments and claim the same outcomes will occur. It’s actually a perfectly reasonable point – there are too many confounding variables.

However, the difficulty is that we do not know how much crying with a non-response is tolerable by a child. It may depend on age, contextual factors, the length of time spent crying, as well as internal factors such as child resilience, and the presence of genetic buffers, variations in cortisol response and a huge number of other variables.

We do not at the current time have a research study that has adequately addressed the question of whether leaving children to cry causes harm, or is completely benign. We know that at some point, a lack of response causes a cascade of emotional, psychological and physiological outcomes. But at what point is this a factor when considering sleep training?

Right now, we certainly do not have a full picture of whether CC and CIO cause harm or not. There is enough evidence for us to be concerned that at some point it potentially could cause harm. My main issue though, is with the prevailing certainty that we have proof of no harm. I am not suggesting that we have definitive proof of harm, but the opposite is equally not true.

I find the widespread acceptance of research that includes incomplete data sets, methodological flaws, lack of population representation, incorrect interpretations, high drop-out rates, and small samples staggering. The bottom line is that the current research does not allow us to make a fully informed decision.

What can we do for parents at the present time that is evidence-based?

I have tried to thoroughly explore the research we have at the current time, and presently am unsatisfied that we can recommend CC or CIO with any certainty or guarantee of a lack of harm. I must be clear here that I am trying to be as unbiased as I can. It is no great secret that I am not a fan of CC or CIO as a sleep strategy, but what I have been attempting to do is explain rationally what my objections are.

However, I am also a realist, a pragmatist and highly compassionate to modern families who are often lacking social support and may be struggling with real and significant problems with finances, short parental leave, mental health, relationships and housing.

To this end, it is my opinion that parents do sometimes need support with sleep. But how can we ensure that sleep support (in the absence of conclusive evidence about behavioural sleep training) is risk-free? I seem to spend most of my time exploring this exact principle, partly because I am unconvinced by the current evidence base around CC and CIO, but also because many parents simply don’t want to utilize these techniques (Sadeh et al, 2016). I now recommend only strategies that do not have any evidence of potential harm:

Provide support scaffolding to families who are struggling – encouraging social, community, and familial support wherever possible, and paid support if desired and financially viable for a family (Teti et al, 2017)

Of course, sometimes families need additional sleep strategies, but there are so many to choose from that do not involve leaving children alone to cry that in the absence of robust research, it seems sensible to suggest strategies that specify parental presence, rather than leaving infants alone.

So, returning to the original question: I would conclude by suggesting that the problem with pitting these opposing viewpoints against each other is that we are getting nowhere from an academic point of view. Meanwhile, the families who need help are not only confused about who is speaking the truth, but are also not getting any more sleep. It’s time to acknowledge that we do not have all the answers, and work towards finding more palatable solutions for tired and desperate families.

Lyndsey Hookway is a paediatric nurse, health visitor, IBCLC and holistic sleep and behaviour coach. She works privately at www.feedsleepbond.com. Lyndsey is a respected International speaker and the Co-founder and Clinical Director of the Holistic Sleep Coaching Program. Her first book – Holistic Sleep Coaching – is out now on Amazon and direct from the publisher.

Douglas, P. S., & Hill, P. S. (2013). Behavioral sleep interventions in the first six months of life do not improve outcomes for mothers or infants: a systematic review. Journal of Developmental & Behavioral Pediatrics, 34(7), 497-507.

Scher, A. (2001). Attachment and sleep: A study of night waking in 12‐month‐old infants. Developmental Psychobiology: The Journal of the International Society for Developmental Psychobiology, 38(4), 274-285.